Spinal tetracaine decreases central nervous system metabolism during somatosensory stimulation in the rat

The influence of spinal tetracaine on central nervous system (CNS) metabolism was determined during nociceptive stimulation. Rats were divided into a halothane group in which the sciatic nerve was stimulated during 0.5 per cent halothane anaesthesia, a tetracaine group in which the sciatic nerve was stimulated during a simultaneous tetracaine spinal and 0.5 per cent halothane anaesthetic, or an awake group. Autoradiographic determination of local spinal cord and cerebral glucose utilization was performed using 14C-2-deoxyglucose. Central nervous system metabolism was greater in the halothane group than the tetracaine and awake groups (P less than 0.05). The only meaningful differences between the tetracaine and awake groups were in two lumbar grey areas at the site of drug administration where metabolism was decreased in the tetracaine/stimulated group. These results indicate that spinal tetracaine effects a decrease in metabolism locally, and attenuates increases in metabolism throughout the CNS observed during somatosensory stimulation.     

EFFECTS OF FENTANYL, DROPERIDOL, AND INNOVAR ON CANINE CEREBRAL METABOLISM AND BLOOD FLOW

The effects of droperidol and fentanyl given individually andin combination (Innovar) on the rate of cerebral oxygen consumption(CMRo,) and cerebral blood flow (c.b.f.) were studied in dogsanaesthetized with nitrous oxide (70 percent) and oxygen. Fentanyl(0.006 mg/kg) decreased both the CMRo, and the c.b.f. (meandecreases at 15 minutes were 18 per cent and 47 percent, respectively).The duration of effect was approximately 30 minutes. Droperidol(0.3 mg/kg) produced a decrease of 40 per cent in c.b.f. dueprimarily to a 30-40 per cent increase in cerebrovascular resistance,and this effect persisted for the period of observation (60minutes). No significant change in CMRo, occurred after droperidolwas administered. With the combination drug (Innovar), the effectswere partially additive. After 15 minutes, CMRo, had decreased23 per cent; c.b.f. had decreased 50 per cent; and cerebralvascular resistance had increased 85 per cent. After 30 minutes,the effects of Innovar were indistinguishable from those ofdroperidol alone. No significant changes occurred in the rateof cerebral glucose consumption or the oxygen-glucose index.The effect of increased and decreased Paooj on c.bi. after Innovarwas compared widi that observed during halothane anaesthesia.With halothane, hypercapnia (Pacoi=60 tnm Hg) increased c.b.f.40 per cent and hypocapnia (Pace = 20 mm Hg) decreased c.b.f.40 per cent. Innovar at normocapnia reduced the c.b.f. 65 percent. With hypercapnia, the c.bi. doubled, but with hypocapnia,little further reduction in c.b.f. occurred. It is concludedthat droperidol is a potent cerebral vasoconstrictor, that thiseffect dominates when it is given in combination with fentanyl,that hypocapnia causes little further reduction in c.b.f., andthat the reduction in c.bi. produced by Innovar is not accompaniedby alterations in normal cerebral metabolic pathways     

Effects of dose and concentration of rectal methohexitone for induction of anaesthesia in children

To investigate the effect of dose and concentration of rectal methohexitone for induction of anaesthesia, 60 children (ASA physical status 1 or 2) undergoing outpatient surgery were studied. Each child was randomly assigned to receive one of three rectal solutions (each containing atropine 0.02 mg X kg-1): Group A - ten per cent methohexitone, 25 mg X kg-1 (n = 20); Group B - ten per cent methohexitone, 15 mg X kg-1 (n = 20); or Group C - one per cent methohexitone, 15 mg X kg-1 (n = 20). After induction of anaesthesia, or a maximum period of 20 minutes following rectal administration of methohexitone, halothane, nitrous oxide, and oxygen were administered by mask. The time to induction of anaesthesia, complications, postanaesthetic recovery scores, and recovery time did not differ significantly among the three groups. The incidence of failed inductions did not differ significantly between Group A (zero per cent) and Group C (ten per cent) but both were significantly less than Group B (45 per cent) (p less than 0.05). Heart rate increased significantly between 10 and 30 minutes after rectal administration of methohexitone and atropine. The authors conclude that ten per cent rectal methohexitone 25 mg X kg-1 and one per cent rectal methohexitone 15 mg X kg-1 are equally effective for induction of anaesthesia in children and both are significantly more effective than ten per cent methohexitone 15 mg X kg-1.     

Intravenous glucose tolerance test during anaesthesia in dogs: insulin response and glucose clearance

To evaluate the insulin response and the rates of disappearance of glucose from plasma during high spinal analgesia and various types of general anaesthesia, a series of intravenous glucose tolerance tests was performed in six dogs. Plasma glucose and insulin levels were measured during the intravenous glucose tolerance tests. Insulinogenic indices were calculated. The values obtained during anaesthesia were compared to those obtained during an unanaesthetized state. The insulinogenic index was increased significantly during high spinal analgesia and thiopentone infusion. Halothane and enflurane anaesthesia decreased the insulinogenic index significantly while Innovar-nitrous oxide also decreased it, but not significantly. These findings suggest that insulin secretion in response to hyperglycaemia is stimulated by spinal analgesia and thiopentone anaesthesia, depressed by halothane and enflurane anaesthesia and unchanged during neuroleptanesthesia. A diuresis was observed in the thiopentone anaesthetic and spinal analgesic groups as compared to the other general anaesthetic groups. Urinary losses of insulin and glucose paralleled urinary output; yet the greatest mean urinary loss of glucose did not exceed 4.5 per cent of the load of glucose administered. Accordingly, 95 per cent of the administered glucose remained within the body, presumably available for utilization.     

Effects of halothane on arrhythmias induced by myocardial ischaemia

The effect of halothane on arrhythmias induced by ischaemia was investigated in rats, isolated perfused rat hearts, and pigs. Responses to the occlusion of the left anterior descending coronary artery were determined in groups (n = 9) of chronically prepared rats treated with no halothane, 0.5, or 1.0 per cent halothane immediately after occlusion; in isolated rat hearts (n = 10) treated with no halothane, 0.5, 1.0, 2.0, or 4.0 per cent halothane for 15 min before and after occlusion; and 20–25 kg pigs (n = 11) anaesthetised with halothane or pentobarbital. The ECG, arrhythmias, blood pressure (BP), heart rate (HR) and extent of infarction were determined in each model. In pigs, left ventricular pressure, dp/dt_max and cardiac output were also measured. In chronically prepared rats, halothane anaesthesia started after occlusion was antiarrhythmic and decreased the incidence of ventricular fibrillation and resulting mortality. In isolated rat hearts, 0.5 or 1.0 per cent halothane had little effect on occlusion-induced arrhythmias. The highest concentration of halothane increased the incidence of ventricular fibrillation both before and after occlusion. Halothane decreased developed ventricular pressure in a dose-dependent manner. In acutely prepared pigs, halothane pre-treatment had no appreciable effect upon occlusion-induced arrhythmias when compared with pentobarbital anaesthesia. Thus, halothane is antiarrhythmic when treatment is initiated after occlusion in the rat but this action is not seen in isolated hearts or intact pigs. The antiarrhythmic action of halothane is, therefore, species and model dependent.     

Effect of halothane,enflurane and isoflurane on the end-systolic pressure-length relationship

Myocardial contractility was measured using the end-systolic pressure-length (ESPL) relationship in dogs subjected to increasing concentrations of halothane (0.5-2 per cent), enflurane (0.77-2.6 per cent) or isoflurane (0.70-2.13 per cent), combined with an infusion 7 micrograms X kg-1 X min-1 of fentanyl, after induction of anaesthesia with 15 mg X kg-1 thiopentone. The relationship between the concentrations of the different drugs and contractility (ESPL) can best be described by ESPL = a + b/(MAC fraction) where "a" is a constant and "b" is the slope of the curve relating ESPL to MAC. At 1.0 MAC values, the ESPL for halothane (69.04 +/- 25.83 mmHg X mm-1) did not differ from that of isoflurane (63.19 +/- 17.36 mmHg X mm-1). However, the myocardial contractility during 1.0 MAC halothane and isoflurane anaesthesia was better preserved than that of enflurane (38.66 +/- 9.73 mmHg X mm-1: p less than 0.01, p less than 0.05 respectively).     

Postoperative vomiting following strabismus surgery in paediatric outpatients: spontaneous versus controlled ventilation

The study was designed to compare the frequency and severity of postoperative vomiting in paediatric out-patients receiving controlled ventilation (IPPV) or breathing spontaneously (SV) during anaesthesia for strabismus repair. One hundred and twenty unpremedicated children (ages 2-12 years) were studied in a randomized fashion. After intravenous induction of anaesthesia and tracheal intubation, patients breathed halothane 1-1.5 per cent inspired and N2O 66 per cent in O2 spontaneously (n = 60), or received IPPV, halothane 0.5-1 per cent, N2O 66 per cent, and pancuronium 0.05 mg.kg-1, which was reversed with neostigmine and atropine (n = 60). The incidence of vomiting with SV was 50 per cent (95 per cent confidence limits: 34.5-65.5 per cent) compared with 40 per cent (24.5-55.5 per cent) with IPPV (p greater than 0.25). Patients in the SV group experiencing emesis had longer operations than those not vomiting (mean +/- SEM = 1.5 +/- 0.1 vs 1.2 +/- 0.1 hours, p less than 0.005). This was not the case with IPPV. There was no correlation between age, sex, duration of surgery, or number of extraocular muscles repaired, and frequency or severity of vomiting or time to discharge. No significant advantage was afforded by IPPV over SV in the present study.     

Haemodynamic effects of atropine during halothane or isoflurane anaesthesia in infants and small children

In this study, two-dimensional and pulsed Doppler echocardiography were used to measure cardiovascular changes before and after IV atropine in 31 infants and small children during halothane (n = 15) or isoflurane (n = 16) anaesthesia. Prior to induction of anaesthesia heart rate (HR), mean blood pressure (MBP), and two0dimensional echocardiographic dimensions of the left ventricle and pulmonary artery bloodflow velocity were measured by pulsed Doppler echocardiography. Cardiovascular measurements were repeated while anaesthesia was maintained at 1.5 MAC halothane (n = 15) or isoflurane (n = 16). Atropine 0.02 mg·kg⁻¹ IV was then administered and two minutes later, a third set of cardiovascular data was obtained. Heart rate decreased during halothane anaesthesia but did not change significantly during isoflurane anaesthesia. Mean blood pressure, cardiac output (CO) and stroke volume (SV) decreased similarly during 1.5 MAC halothane or isoflurane anaesthesia. Ejection fraction (EF) decreased and left ventricular end-diastolic volume (LVEDV) increased significantly in bothgroups, but decreases in EF (32 ± 5 percentvs18 ± 5 per cent) and increases in LVEDV (18 ± 7 per cent vs7 ± 5 per cent) were significantly greater during halothane than during isoflurane anaesthesia. Following atropine, HR increased more in the patients maintained with halothane (31 ± 6 per cent), than during isoflurane anaesthesia (18 ± 5 per cent). Atropine increased CO in both groups of patients, but SV and EF remained unchanged. When compared with awake values, HR increased similarly and significantly (18 ± 4 per cent) following atropine in both groups, and CO returned to control levels. Halothane decreased EF and increased LVEDV more than isoflurane at 1.5 MAC end— expired anaesthetic levels. Atropine did not diminish the myocardial depression produced by halothane or isoflurane. The increase in CO following atropine during halothane and isoflurane anaesthesia in infants and small children is the result of increases in HR alone. Nous avons utilisé un appareil à échocardiographie bi-dimensionnelle couplé à un Doppler pulsé chez des bébés et de jeunes enfants pour évaluer l’impact hémodynamique de l’halothane (n = 15) et de l’isoflurane (n = 16) et la modification possible de ces effets par l’atropine. Nous avons mesure la frequence cardiaque (FC), la pression artérielle moyenne (PAM), la dimension de la cavité ventriculaire gauche (par écho bi-dimensionnelle) et la vélocité du flot sanguin pulmonaire (par Doppler) et ce, en trois occasions soit avant l’induction, après l’instauration de 1.5 MAC d’halothane ou d’isoflurane et finalement, deux minutes après l’injection IV de 0.02 mg·kg⁻¹ d’atropine. On ne nota une baisse de la frequence cardiaque qu’avec l’halothane tandis que la PAM, le débit cardiaque (DC) et le volume d’éjection (VE) diminuaient autant avec l’un ou l’autre anesthésique. La diminution de la fraction d’éjection (FE) et l’augmentation du volume télédiastolique du ventricule gauche (VTDVG) significatives pour les deux groupes, étaienl plus marqué avec l’halothane qu’avec l’isoflurane: FE 32 ± 5 pour cent vs18 ±5 pour cent; VTDVG 18 ± 7 pour cent vs 7 ± 5 pour cent. Avec l’atropine, la FC monta plus dans le groupe halothane (31 ± 6 pour cent) que dans le groupe isoflurane (18 ± 5 pour cent), le DC augmentant dans les deux groupes, alors que le VE et la FE demeuraient inchangés. Comparée aux mesures pré-induction, l’atropine amenait une hausse significative de la FC, semblable dans les deux groupes (18 ± 4 pour cent) et restaurait le DC. Donc, chez les bebes et les jeunes enfants, a 1.5 MAC, l’halothane diminue la FE et augmente le VTDVG plus que ne le fait l’isoflurane. L’atropine ne modifie pas la depression myocardique et elle ne restaure le DC que par une hausse de la FC.

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Supported by PHS Grant No. 8507300 from the College of Medicine, University of Iowa Hospital, Iowa City, IA.     

Heart rate response to atropine in humans anaesthetized with five different techniques

Atropine, 0.01 mg.kg-1, was given intravenously before the start of surgery to 169 patients who were anaesthetized with one of five different techniques; halothane, enflurane, cervical epidural, lumbar epidural or narcotic anaesthesia in addition to nitrous oxide and oxygen. Atropine produced a significant increase in heart rate (HR) within 1 min in all patients studied; the HR increases in patients anaesthetized with halothane (37 +/- 11 beats.min-1, n = 37) or narcotic (34 +/- 12 beats.min-1, n = 30) were significantly greater than in those anaesthetized with enflurane (25 +/- 10 beats.min-1, n = 35; P less than 0.01) or epidural anaesthesia. Because of the presence of an acute cardiac sympathectomy, the patients who received cervical epidural anaesthesia were expected to have different responses to the atropine. However, there was no significant difference in the HR increases between the patient groups with cervical (19 +/- 12 beats.min-1, n = 32) and lumbar (22 +/- 8 beats.min-1, n = 35) epidural anaesthesia. Atropine also produced a small but significant increase in arterial pressure in all five groups of patients. These results suggest that the cardiac responses to atropine may differ depending on the individual anaesthetic agent used, and are likely dependent upon the agent's effect on autonomic nervous system activity.     

Changes in myocardial oxygen consumption,efficiency and haemodynamics when systemic pressure is increased during morphine and added halothane anaesthesia in dogs

Depression of left ventricular function by the combination of halothane anaesthesia and increased ventricular afterload may undesirably reduce stroke volume and increase myocardial oxygen consumption by increasing ventricular wall stress. To investigate this possibility we studied six dogs instrumented to measure systemic and left ventricular pressures, ascending aortic and left anterior descending coronary artery flows and external left ventricular diameters. We sampled arterial and coronary sinus blood gases and oxygen contents. During morphine anaesthesia (4mg·kg^-1 intravenously with hourly supplements of 0.1 mg·kg^-1) and during added halothane anaesthesia (1.5 per cent end tidal) we measured systemic pressure, heart rate, stroke volume, stroke work, cardiac output, left ventricular end diastolic pressure and diameter and myocardial oxygen consumption. After infusing phenylephrine (0.02 mg/ml) to increase systolic pressure to 23.28 kPa (175 torr) we repeated measurements in both groups. We found that added halothane depressed systemic pressures (52 per cent), stroke volume (30 per cent), and myocardial oxygen consumption (46 per cent) compared to morphine alone. When afterload was increased with phenylephrine, stroke volume (20 per cent), cardiac output (25 per cent) and myocardial efficiency (47 per cent) were further depressed during added halothane anaesthesia compared to control halothane anaesthesia. Left ventricular end diastolic diameter (5 per cent) and pressure (320 per cent) were significantly increased by added afterload, compared to the control added halothane state. Conversely, increased afterload produced few changes during morphine anaesthesia alone. However, at comparable systemic pressures, myocardial oxygen consumption was similar during both anaesthetic states. We conclude that during added halothane anaesthesia increased afterload decreases stroke volume and myocardial efficiency. Cardiac output is reduced without increased myocardial oxygen consumption compared to morphine anaesthesia at comparable afterload states. In patients with already compromised cardiac output, further depression of stroke volume by increased ventricular afterload during halothane anaesthesia may be deleterious.     

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2-reactivity during craniotomy for supratentorial cerebral tumours in halothane anaesthesia. A dose-response study

Fourteen patients were studied during craniotomy for small supratentorial cerebral tumours. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice by a modification of the Kety-Schmidt technique using 133Xe intravenously. Anaesthesia was induced with thiopental 4-6 mg kg-1, fentanyl and pancuronium, and maintained with an inspiratory halothane concentration of 0.45% in nitrous oxide 67% at a moderate hypocapnic level. In one group of patients (n = 7) the inspiratory halothane concentration was maintained at 0.45% throughout anaesthesia. About 1 h after induction of anaesthesia CBF and CMRO2 averaged 35 +/- 2 ml 100 g-1 min-1 and 2.7 +/- 0.3 ml O2 100 g-1 min-1 (mean +/- s.c. mean), respectively. During repeat studies 1 h later CBF and CMRO2 did not change. In another group of patients (n = 7) an increase in halothane concentration from 0.45% to 0.90% was associated with a significant decrease in CMRO2 from 2.3 +/- 0.1 to 2.0 +/- 0.1 ml O2 100 g-1 min-1. The CO2-reactivity measured after the second flow measurement was preserved. It is concluded that halothane in this study induces a dose-dependent decrease in cerebral metabolism, an increase in CBF while CO2-reactivity is maintained.     

Foetal responses to acute haemorrhage under halothane anaesthesia

The effect of halothane anaesthesia on the foetal responses to acute haemorrhage was studied in chronically prepared ewes. An average of 27.9 ml·kg^-1of foetal blood was withdrawn resulting in an acute 20 per cent decrease in mean arterial pressure which returned toward the control value after 186 seconds. After the blood loss, cardiac output was reduced by 26.1 per cent and heart rate decreased by 26 per cent. Blood flows to the kidneys, placenta and musculoskeletal structures were reduced by 247, 38.2 and 35.3 per cent respectively but flow to the brain increased by 30 per cent. Reinfusion of lost blood, corrected flow reductions and the supply to the gastrointestinal organs increased above control values. This study showed that foetal lambs were able to tolerate an acute blood loss under halothane anaesthesia. An adequate perfusion pressure and blood flow to critical organs, such as the brain was maintained by increasing systemic vascular resistance. The compensation, however, was incomplete. Placental blood flow, maternal-foetal gas exchanges, and redistribution of cardiac output away from gastrointestinal tract and skin were impaired.     

Induction reflex actions with intravenous nalbuphine as an adjunct to isoflurane

Ninety unpremedicated patients undergoing mask anaesthesia were assigned to one of three groups according to the volatile anaesthetic and the acute intravenous premedication administered. Group I received saline placebo as premedication and halothane by inhalation. Group II received saline placebo and isoflurane by inhalation. Group III received nalbuphine 0.1 mg.kg-1 IV as premedication and isoflurance by inhalation. Mean time to loss of consciousness (71 sec) did not differ among groups. The dosage of thiopentone required to induce loss of consciousness was decreased by 15 per cent (from 3.9 to 3.3 mg.kg-1) by nalbuphine premedication (P less than 0.05), and time to induction of surgical anaesthesia using isoflurane was decreased by 15 per cent (P less than 0.05). The incidence of reflex actions (coughing, laryngospasm, breath holding, hiccoughs and movement) during induction was no different in the saline-premedicated halothane or isoflurane groups. Acute intravenous nalbuphine premedication decreased significantly the incidence of reflex actions during induction of isoflurane anaesthesia from 77 per cent to 37 per cent (P less than 0.02). Desaturation episodes (SaO2 less than 90 per cent) were more frequent with isoflurane inductions compared with halothane (55 per cent vs 17 per cent, P less than 0.01). Apnoeic episodes accounted for the majority of desaturations associated with nalbuphine premedication, while excitatory reflexes (coughing and laryngospasm) accounted for more desaturations with isoflurane alone.     

Clonidine prolongs canine tetracaine spinal anaesthesia

Using a randomized blind cross-over design, the comparative efficacy of clonidine in prolonging tetracaine spinal anaesthesia was studied in six mongrel dogs. Lumbar subarachnoid injections (1 ml) of: tetracaine 4 mg with clonidine 150 micrograms, tetracaine 4 mg with epinephrine 200 micrograms, tetracaine 4 mg, clonidine 150 micrograms, epinephrine 200 micrograms, and five per cent dextrose in H2O (vehicle) were administered randomly to each animal at 5-7 day intervals. Subarachnoid tetracaine produced a motor blockade of 186 +/- 58 (mean +/- SEM) min. Both clonidine and epinephrine produced a similar prolongation of tetracaine motor blockade, 135 per cent (p less than 0.01) and 116 per cent (p less than 0.05) respectively, compared with tetracaine alone. No motor blockade was observed in dogs receiving clonidine, epinephrine or five per cent dextrose in H2O. The addition of clonidine to tetracaine spinal anaesthesia produced a significant increase in duration of sensory blockade, 56 per cent (p less than 0.01) and 107 per cent (p less than 0.01) respectively, when compared to tetracaine with and without epinephrine. Subarachnoid clonidine alone produced a sensory blockade of 76 +/- 17 minutes, while only one animal receiving subarachnoid epinephrine had a sensory blockade (40 minutes). No neurologic deficits were observed in any of the animals. The study concludes that during spinal anaesthesia with tetracaine in dogs, clonidine is as effective as epinephrine in prolonging motor blockade, but is more effective in prolonging sensory blockade.     

The Effect of Halothane Anaesthesia upon Cerebral Oxygen Consumption in the Rat

The influence of halothane (0.6 and 2%) upon cerebral (cortical) blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) was studied in artificially ventilated rats, using a modified technique of Kety & Schmidt (1948). The values obtained in halothane anaesthesia were compared to those recorded in nitrous oxide anaesthesia, or to those measured in unanesthetized animals given an analgesic drug (fentanyl citrate). Although it could be confirmed that halothane induces vasodilatation in the brain, there were relatively small differences in CBF between the groups. The results demonstrate that, in the rat, halothane depresses CMRo2 in a dose-dependent way. With 0.6% halothane, CMRo2 was reduced by 20-30% and, with 2% halothane, CMRo2 was reduced by about 50%. Thus, in the rat the effect of 2% halothane upon metabolic rate is comparable to that observed in barbiturate anaesthesia.     

OXYGEN AND ANAEMIA: THEIR EFFECTS IN MICE, ON INDUCTION TIME AND SURVIVAL TIME WITH HALOTHANE ANAESTHESIA

This paper reports the results of five studies on female miceto investigate the effects of halothane anaesthesia in air and100 per cent oxygen on induction time, survival time and sensitivityto halothane, in bled and unbled mice. Studies on the effectof anaemia on induction time and survival time showed that reductionsof haemoglobin content significantly reduced induction timesin mice anaesthetized with 10 per cent halothane in air and100 per cent oxygen (2 1./min), but did not significandy affectthe survival times in the same groups of mice. The use of 100per cent oxygen instead of air as the anaesthetic vehicle causeda highly significant increase in induction times and survivaltimes in both bled and unbled mice. Toxicity studies to determinethe halothane concentrations required to kill 50 per cent and99 per cent of mice in 30 minutes were used to confirm the resultsof the above survival studies. One study showed that in unbledmice, the mice were significantly more sensitive to halothane/airanaesthesia than to halothane/100 per cent oxygen anaesthesia.Other studies showed that a mean haemoglobin reduction of 31per cent did not significandy affect the mouse sensitivity tohalothane/100 per cent oxygen anaesthesia, but a reduction of45 per cent significantly increased the sensitivity of the bledmice to halothane/100 per cent oxygen. Body weight was shownto have a highly significant effect on induction time and survivaltime with 10 per cent halothane/100 per cent oxygen, but a non-significanteffect with 10 per cent halothane/air.     

Local spinal cord blood flow and glucose utilization during spinal anesthesia with bupivacaine in conscious rats

The author studied in conscious rats the local spinal blood flow (SCBF) and metabolic effects of intrathecally administered bupivacaine. Fourteen rats received 0.75% bupivacaine, 15 microliters, through a chronically implanted lumbar subarachnoid catheter. Twelve control animals were treated identically, except that they received only an equal volume of saline intrathecally. Ten minutes after intrathecal drug injection, either local SCBF or glucose utilization was measured in the lumbar spinal cord of seven experimental and six control animals with the quantitative autoradiographic iodo-[14C]antipyrine or 2-[14C]deoxyglucose methods, respectively. Intrathecal bupivacaine produced a limp tail, absent hindlimb withdrawal to pinch, and 25-30 min of analgesia on the tail-flick test. Mean arterial blood pressure decreased 14% (P less than 0.01) after bupivacaine was administered, but there was no change in arterial blood gases, pH, or rectal temperature. Subarachnoid bupivacaine reduced both local SCBF and glucose utilization, but the SCBF effect was larger. Local SCBF decreased 27-34% (P less than 0.01) in all five spinal gray and three white matter areas measured, and there was little regional variability in the response. The reduction in spinal glucose utilization was regionally selective and less marked. For example, glucose utilization decreased 15% (P less than 0.05) and 21% (P less than 0.05) in lateral and anterior spinal white matter, respectively, but only decreased approximately 3% in laminae I-III and dorsal white matter (P greater than 0.1). A trend toward metabolic depression was also evident in laminae VIII (-15%, P = 0.06), VII (-13%, P = 0.09), and IV-VI (-11%, P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral blood flow and oxygen consumption during isoflurane and halothane anesthesia in man

In 13 patients, the effects on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) of isoflurane and halothane administered in a clinically relevant situation were studied. Measurements were performed during fentanyl/nitrous oxide (65%) anesthesia together with moderate hyperventilation (PaCO2 approx 4.5 kPa), and repeated after addition of 0.65 MAC of isoflurane (n = 6) or halothane (n = 7). CBF was measured after intravenous administration of 133xenon and CMRO2 was calculated from the arterial venous differences of oxygen content (AVDO2) determined in arterial and jugular venous bulb blood. CBF and CMRO2 (means +/- s.e. mean) determined prior to administration of volatile agents were 28 +/- 5 ml x 100(-1) x min-1 and 2.0 +/- 0.3 ml x 100 g-1 x min-1, respectively, in the isoflurane group. In the halothane group, CBF was 25 +/- 0.4 ml x 100 g-1 x min-1 and CMRO2 was 2.0 +/- 0.4 ml x 100 g-1 x ml-1. There were no significant intergroup differences. Isoflurane did not change CBF, whereas halothane produced an increase of 36% (P less than 0.05) compared to values obtained during fentanyl/N2O anesthesia. In addition, isoflurane caused a further decrease in CMRO2 of 12% (P less than 0.01) as compared to a 20% increase (P less than 0.05) with halothane. The cerebral metabolic depression caused by the short-acting anesthetic induction agents would be expected to decrease with time, and could partly explain the observed increase in CMRO2 produced by halothane. The study suggests that the cerebrovascular and metabolic properties of isoflurane differ from those of halothane, also in man.     

CEREBRAL VASODILATATION BY HALOTHANE ANAESTHESIA IN MAN AND ITS POTENTIATION BY HYPOTENSION AND HYPERCAPNIA

In ten young normal adults the cerebral blood flow and oxygenuptake during normotensive and normocapnic halothane anaesthesia(1 per cent) were studied by means of the ⁸⁵Kr inhalation method.Compared with a similar group studied when awake, a significantincrease of 27 per cent in cerebral blood flow was found duringanaesthesia while the oxygen uptake was reduced by 26 per cent.After discussing previous conflicting reports, it is concludedthat halothane per se acts as a cerebral vasodilator. Ten patientsfrom the neurological service with and without cerebrovasculardisease were studied when awake and during hypotensive hypercapnichalothane anaesthesia (1 per cent). In five cases a third studywas made during either hypotension (three cases) or hypercapnia(two cases) alone. Cerebral blood flow was measured by the ¹³³Xeinjection method. The results suggested a potentiation of thecerebral vasodilatation of halothane by hypotension and/or hypercapniaeven in patients with cerebrovascular disease. The very highblood flows found during normotensive, moderately hypercapnichalothane anaesthesia indicated a sort of controlled cerebralhyperoxygenation, the application of which is discussed.     

The cerebral arterio-venous oxygen content differences (AVDo2) during halothane and neurolept anaesthesia in patients subjected to craniotomy

In 20 patients subjected to craniotomy for supratentorial cerebral tumours, the haemodynamic changes during halothane and neurolept anaesthesia were evaluated by measuring mean arterial blood pressure (MABP) and cerebral arterio-venous oxygen content differences (AVDO2) repeatedly during the operation. Ten patients were given 0.5% halothane anaesthesia and ten patients neurolept anaesthesia. MABP, AVDO2 and PaCO2 were measured after induction of anaesthesia, before and after incision, after opening and closure of the dura, at the time of extubation and 1 h later. Concerning MABP and PaCO2, no significant difference between the two groups was found. In both groups an increase in MABP was observed after incision (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group) and in the neurolept group after extubation (P less than 0.01). In both groups a decrease in AVDO2 was observed after incision (P less than 0.01) and after extubation (P less than 0.01 in the neurolept group and P less than 0.05 in the halothane group). During the operation AVDO2 values were significantly higher in the neurolept group (P less than 0.05). The results indicate that even a moderate increase in MABP after incision during neuroanaesthesia affects AVDO2 values, suggesting an increase in cerebral blood flow. The study suggests that autoregulation of cerebral blood flow might be better preserved during neurolept anaesthesia. A state of hyperperfusion of the brain after extubation was unveiled in both groups.